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  1. Article: Loss of Progranulin Results in Increased Pan-Cathepsin Activity and Reduced LAMP1 Lysosomal Protein.

    Anderson, Abigail / Tansey, Malú G

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Mutations in the progranulin (PGRN) encoding gene, ...

    Abstract Mutations in the progranulin (PGRN) encoding gene,
    Language English
    Publishing date 2023-07-16
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.07.15.549151
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Is LRRK2 the missing link between inflammatory bowel disease and Parkinson's disease?

    Herrick, Mary K / Tansey, Malú G

    NPJ Parkinson's disease

    2021  Volume 7, Issue 1, Page(s) 26

    Abstract: Links that implicate the gastrointestinal system in Parkinson's disease (PD) pathogenesis and progression have become increasingly common. PD shares several similarities with Crohn's disease (CD). Intestinal inflammation is common in both PD and CD and ... ...

    Abstract Links that implicate the gastrointestinal system in Parkinson's disease (PD) pathogenesis and progression have become increasingly common. PD shares several similarities with Crohn's disease (CD). Intestinal inflammation is common in both PD and CD and is hypothesized to contribute to PD neuropathology. Mutations in leucine-rich repeat kinase 2 (LRRK2) are one of the greatest genetic contributors to PD. Variants in LRRK2 have also been associated with increased incidence of CD. Since its discovery, LRRK2 has been studied intensely in neurons, despite multiple lines of evidence showing that LRRK2 is highly expressed in immune cells. Based on the fact that higher levels of LRRK2 are detectable in inflamed colonic tissue from CD patients and in peripheral immune cells from sporadic PD patients relative to matched controls, we posit that LRRK2 regulates inflammatory processes. Therefore, LRRK2 may sit at a crossroads whereby gut inflammation and higher LRRK2 levels in CD may be a biomarker of increased risk for sporadic PD and/or may represent a tractable therapeutic target in inflammatory diseases that increase risk for PD. Here we will focus on reviewing how PD and CD share overlapping phenotypes, particularly in terms of LRRK2 in the context of the immune system, that could be targeted in future therapies.
    Language English
    Publishing date 2021-03-09
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2819218-7
    ISSN 2373-8057
    ISSN 2373-8057
    DOI 10.1038/s41531-021-00170-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Infection triggers symptoms similar to those of Parkinson's disease in mice lacking PINK1 protein.

    Herrick, Mary K / Tansey, Malú G

    Nature

    2019  Volume 571, Issue 7766, Page(s) 481–482

    MeSH term(s) Animals ; Mice ; Mitochondria ; Parkinson Disease ; Protein Kinases
    Chemical Substances Protein Kinases (EC 2.7.-)
    Language English
    Publishing date 2019-11-20
    Publishing country England
    Document type News ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-019-02094-6
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  4. Article ; Online: LRRK2 regulation of immune-pathways and inflammatory disease.

    Wallings, Rebecca L / Tansey, Malú G

    Biochemical Society transactions

    2019  Volume 47, Issue 6, Page(s) 1581–1595

    Abstract: Mutations in the leucine-rich-repeat kinase 2 (LRRK2) gene are associated with familial and sporadic cases of Parkinson's disease but are also found in immune-related disorders such as inflammatory bowel disease, tuberculosis and leprosy. LRRK2 is highly ...

    Abstract Mutations in the leucine-rich-repeat kinase 2 (LRRK2) gene are associated with familial and sporadic cases of Parkinson's disease but are also found in immune-related disorders such as inflammatory bowel disease, tuberculosis and leprosy. LRRK2 is highly expressed in immune cells and has been functionally linked to pathways pertinent to immune cell function, such as cytokine release, autophagy and phagocytosis. Here, we examine the current understanding of the role of LRRK2 kinase activity in pathway regulation in immune cells, drawing upon data from multiple diseases associated with LRRK2 to highlight the pleiotropic effects of LRRK2 in different cell types. We discuss the role of the bona fide LRRK2 substrate, Rab GTPases, in LRRK2 pathway regulation as well as downstream events in the autophagy and inflammatory pathways.
    MeSH term(s) Animals ; Humans ; Immune System/physiology ; Inflammation/immunology ; Inflammation/physiopathology ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/physiology ; Mutation
    Chemical Substances Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
    Language English
    Publishing date 2019-12-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20180463
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    Zs.A 944: Show issues Location:
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  5. Article ; Online: Publisher Correction: Peripheral and central immune system crosstalk in Alzheimer disease - a research prospectus.

    Bettcher, Brianne M / Tansey, Malú G / Dorothée, Guillaume / Heneka, Michael T

    Nature reviews. Neurology

    2021  Volume 17, Issue 11, Page(s) 724

    Language English
    Publishing date 2021-10-08
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-021-00579-5
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    Zs.A 6257: Show issues Location:
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  6. Article ; Online: Peripheral and central immune system crosstalk in Alzheimer disease - a research prospectus.

    Bettcher, Brianne M / Tansey, Malú G / Dorothée, Guillaume / Heneka, Michael T

    Nature reviews. Neurology

    2021  Volume 17, Issue 11, Page(s) 689–701

    Abstract: Dysregulation of the immune system is a cardinal feature of Alzheimer disease (AD), and a considerable body of evidence indicates pathological alterations in central and peripheral immune responses that change over time. Considering AD as a systemic ... ...

    Abstract Dysregulation of the immune system is a cardinal feature of Alzheimer disease (AD), and a considerable body of evidence indicates pathological alterations in central and peripheral immune responses that change over time. Considering AD as a systemic immune process raises important questions about how communication between the peripheral and central compartments occurs and whether this crosstalk represents a therapeutic target. We established a whitepaper workgroup to delineate the current status of the field and to outline a research prospectus for advancing our understanding of peripheral-central immune crosstalk in AD. To guide the prospectus, we begin with an overview of seminal clinical observations that suggest a role for peripheral immune dysregulation and peripheral-central immune communication in AD, followed by formative animal data that provide insights into possible mechanisms for these clinical findings. We then present a roadmap that defines important next steps needed to overcome conceptual and methodological challenges, opportunities for future interdisciplinary research, and suggestions for translating promising mechanistic studies into therapeutic interventions.
    MeSH term(s) Alzheimer Disease/immunology ; Alzheimer Disease/physiopathology ; Alzheimer Disease/therapy ; Animals ; Humans ; Immune System/physiopathology ; Research
    Language English
    Publishing date 2021-09-14
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-021-00549-x
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    Zs.A 6257: Show issues Location:
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  7. Article: The gut-brain axis: is intestinal inflammation a silent driver of Parkinson's disease pathogenesis?

    Houser, Madelyn C / Tansey, Malú G

    NPJ Parkinson's disease

    2017  Volume 3, Page(s) 3

    Abstract: The state of the intestinal environment can have profound effects on the activity of the central nervous system through the physiological contributions of the microbiota, regulation of intestinal barrier function, and altered activity of peripheral ... ...

    Abstract The state of the intestinal environment can have profound effects on the activity of the central nervous system through the physiological contributions of the microbiota, regulation of intestinal barrier function, and altered activity of peripheral neurons. The common language employed for much of the gut-brain communication is the modulation of immune activity. Chronic proinflammatory immune activity is increasingly being recognized as a fundamental element of neurodegenerative disorders, and in Parkinson's disease, inflammation in the intestine appears particularly relevant in pathogenesis. We review the evidence that intestinal dysfunction is present in Parkinson's disease and that it may reflect the earliest manifestations of Parkinson's disease pathology, and we link these findings to dysregulated immune activity. Based on this, we present a model for Parkinson's disease pathogenesis in which the disorder originates in the intestine and progresses with inflammation as its underlying mechanism. More in-depth investigations into the physiological mechanisms underlying peripheral pre-motor symptoms in Parkinson's disease are expected to lead to the development of novel diagnostic and therapeutic measures that can slow or limit progression of the disease to more advanced stages involving debilitating motor and cognitive symptoms.
    Language English
    Publishing date 2017-01-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2819218-7
    ISSN 2373-8057
    ISSN 2373-8057
    DOI 10.1038/s41531-016-0002-0
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  8. Article ; Online: Challenges in Passive Immunization Strategies to Treat Parkinson Disease.

    Manfredsson, Fredric P / Tansey, Malú G / Golde, Todd E

    JAMA neurology

    2018  Volume 75, Issue 10, Page(s) 1180–1181

    MeSH term(s) Humans ; Immunization, Passive ; Parkinson Disease ; alpha-Synuclein
    Chemical Substances alpha-Synuclein
    Language English
    Publishing date 2018-06-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2702023-X
    ISSN 2168-6157 ; 2168-6149
    ISSN (online) 2168-6157
    ISSN 2168-6149
    DOI 10.1001/jamaneurol.2018.0346
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    Ui II Zs.191: Show issues Location:
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  9. Article: α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson's Disease Pathogenesis.

    Butkovich, Laura M / Houser, Madelyn C / Tansey, Malú G

    Frontiers in neuroscience

    2018  Volume 12, Page(s) 626

    Abstract: α-synuclein (α-syn) pathology and loss of noradrenergic neurons in the locus coeruleus (LC) are among the most ubiquitous features of Parkinson's disease (PD). While noradrenergic dysfunction is associated with non-motor symptoms of PD, preclinical ... ...

    Abstract α-synuclein (α-syn) pathology and loss of noradrenergic neurons in the locus coeruleus (LC) are among the most ubiquitous features of Parkinson's disease (PD). While noradrenergic dysfunction is associated with non-motor symptoms of PD, preclinical research suggests that the loss of LC norepinephrine (NE), and subsequently its immune modulatory and neuroprotective actions, may exacerbate or even accelerate disease progression. In this review, we discuss the mechanisms by which α-syn pathology and loss of central NE may directly impact brain health by interrupting neurotrophic factor signaling, exacerbating neuroinflammation, and altering regulation of innate and adaptive immune cells.
    Language English
    Publishing date 2018-09-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2411902-7
    ISSN 1662-453X ; 1662-4548
    ISSN (online) 1662-453X
    ISSN 1662-4548
    DOI 10.3389/fnins.2018.00626
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  10. Article ; Online: Immune system responses in Parkinson's disease: Early and dynamic.

    Tansey, Malú G / Romero-Ramos, Marina

    The European journal of neuroscience

    2018  Volume 49, Issue 3, Page(s) 364–383

    Abstract: The neuropathological hallmarks of Parkinson's disease (PD) are the degeneration and death of dopamine-producing neurons in the ventral midbrain, the widespread intraneuronal aggregation of alpha-synuclein (α) in Lewy bodies and neurites, ... ...

    Abstract The neuropathological hallmarks of Parkinson's disease (PD) are the degeneration and death of dopamine-producing neurons in the ventral midbrain, the widespread intraneuronal aggregation of alpha-synuclein (α) in Lewy bodies and neurites, neuroinflammation, and gliosis. Signs of microglia activation in the PD brain postmortem as well as during disease development revealed by neuroimaging, implicate immune responses in the pathophysiology of the disease. Intensive research during the last two decades has advanced our understanding of the role of these responses in the disease process, yet many questions remain unanswered. A transformative finding in the field has been the confirmation that in vivo microglia are able to respond directly to pathological a-syn aggregates but also to neuronal dysfunction due to intraneuronal a-syn toxicity well in advance of neuronal death. In addition, clinical research and disease models have revealed the involvement of both the innate and adaptive immune systems. Indeed, the data suggest that PD leads not only to a microglia response, but also to a cellular and humoral peripheral immune response. Together, these findings compel us to consider a more holistic view of the immunological processes associated with the disease. Central and peripheral immune responses aimed at maintaining neuronal health will ultimately have consequences on neuronal survival. We will review here the most significant findings that have contributed to the current understanding of the immune response in PD, which is proposed to occur early, involve peripheral and brain immune cells, evolve as neuronal dysfunction progresses, and is likely to influence disease progression.
    MeSH term(s) Animals ; Dopaminergic Neurons/immunology ; Humans ; Immune System/physiopathology ; Microglia/immunology ; Parkinson Disease/immunology ; Parkinson Disease/physiopathology
    Language English
    Publishing date 2018-12-10
    Publishing country France
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 645180-9
    ISSN 1460-9568 ; 0953-816X
    ISSN (online) 1460-9568
    ISSN 0953-816X
    DOI 10.1111/ejn.14290
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